ECC2- SA Intoxications

• anticoagulant rodenticide: hydrocoumarins, indanediones
• neurotoxin rodenticide: bromethalin
• hypercalcemia (vit D3) rodenticide: cholicalciferol

• what type of rodenticide was ingested
• when was the first possible exposure

blocks vitamin K reductase, causing cavitary bleeding

• readily absorbed from GI tract
• peak blood level in 1-12 hours
• undergoes enterohepatic recycling

• clinical hemorrhage 2-3 days following ingestion
• cavitary bleeding most common
• hemorrhagic shock

PT (which tests the extrinsic coagulation pathway, factor VII, which has the shortest half life)- will be prolonged PT at 48 hour mark if a toxic dose was consumed

alteration in coagulation times and clinical signs will not yet be present b/c carboxylates vit K factors will still be present in circulation

• emesis
• decontamination- repeated activated charcoal for 24 hours
• if PT is prolonged at 48 hour mark without clinical bleeding--> oral vit K supplementation for 30 days (recheck PT 48 hours after discontinuing vit K)
• WITH clinical bleeding--> fresh frozen plasma, frozen plasma, cryosupernatant, whole blood, packed RBCs

• replacement of active vit K dependent clotting factors
• replace exogenous vit K
• replace RBCs if bleeding severely

• FFP: contains all clotting factors
• frozen plasma: contains factors II, VII, IX, and X
• cryosupernatant: contains factors II, VII, IX, and X
• whole blood: contains RBCs, all clotting factors, and platelets
• packed RBCs: only for red cell replacement

inhibits oxidative phosphorylation--> decreases ATP production in the CNS--> malfunction of ATP-dependent ion pump--> influx of sodium and fluid--> cerebral edema

• enterohepatic recycling
• very long half life/ prolonged effects

• [within 2-24hrs]
• CNS stimulation or depression
• abnormal behavior
• hyperesthia
• hyperthermia
• focal or generalized motor seizures
• CNS abnormalities
• hind climb paralysis, ataxia, tremors

• ataxia
• paresis
• loss of proprioception and deep pain
• hyperreflexia
• UMN bladder
• mild to severe CNS depression
• focal or generalized motor seizures
• abnormal body postures (schiff-sherrington, decerebrate)

0.25-1mg/kg

• emesis (if exposed within the last 2-4 hours)
• decontamination (repeated activated charcoal for 24-48 hours)
• mannitol (decrease cerebral edema)
• anticonvulsant therapy
• methocarbamol for tremors

high dose of cholecalciferol results in increased Ca absorption, increased urinary Ca reabsorption and increased bone mineralization--> severe hypercalcemia

• enterohepatic recycling
• terminal half life is weeks to months due to high fat solubility
• hypercalcemia can persist for weeks

• [usually 36hr post ingestion]
• depression/ weakness
• GI upset
• PU/PD
• lethargic
• acute renal failure
• cardiac arrhythmias
• seizures

• emesis
• decontamination (repeated activated charcoal for 24 hours)
• reduction of hypercalcemia with fluid therapy, furosemide, +/- calcitonin, bisphosphonates (decreases osteoclastic behavior), steroids (reduce GI absorption of Ca), phosphorous binders

reversible neurotoxin that alters the voltage sensitive sodium channel, leading to disruption of their function

• fat soluble
• toxicity enhanced by carriers (alcohols, solvents)
• cats are more sensitive

• immune-mediated hypersensitivity- dermal manifestation
• neurotoxicity- muscle tremors, ataxia, seizures, death
• topical and oral stimulation- hypersalivation, paw flicking, ear twitching, hyperesthia, decreased activity, vomiting, diarrhea

• oral exposure- decontaminate
• allergic skin reaction- diphenhydramine
• neurologic reaction- muscle tremors treated with methocarbamol, seizures treated with anticonvulsants
• aggressive supportive care

• CO binds hemoglobin to create carboxyhemoglobin, blocks binding of oxygen--> cellular hypoxemia 
• direct cytotoxicity due to altered cellular respiration--> free radical formation--> cell death

• dyspnea
• nausea/ vomiting
• dizziness
• tachycardia
• arrhythmias
• weakness
• ataxia
• seizures
• syncope
• hypotension
• red MMs
• coma

• CO-oximetry: confirms CO toxicity by measuring the amount of hemoglobin, oxygen saturation, and percentage of CO-Hgb
• arterial blood sample: PaO2 will represent dissolved oxygen in blood d/t oxyhemoglobin curve being shifted to the left; monitor response to therapy this way
• [pulse ox: not accurate, CO-Hgb absorbs the same wavelength as O-Hgb]

• oxygen supplementation
• supportive care

• EG itself is not toxic
• its metabolites from the liver result in clinical disease by forming oxalates, which are nephrotoxic and result in mineralization of renal tissue

• 30 min: nausea and vomiting, CNS depression, ataxia, LMN signs in limbs, muscle fasiculations, PU/PD
• 24-72 hours: signs of AKI- depression, anorexia, vomiting, seizures, pytalism, oral ulceration, and coma
• 72-96 hours: anuria, cats may have swollen painful kidneys

• history
• elevated osmolal gap (1 hour following ingestion and remain elevated for 18 hours) [2(Na+K) + (BUN/2.8) + (glucose/18)]
• high anion gap (within 3 hours of ingestion) [(Na+K)- (Cl+HCO3)]
• urinalysis: calcium oxalate crystals (within 3-6 hours), isosthenuria
• also EG test kits available
• biochem: azotemia, hyperPh, hyperK
• abdominal US: halo sign/ hyperechoic renal cortex

• 4-MP or fomepizole (alcohol dehydrogenase inhibitor, block conversion of EG to toxic metabolites)
• ethanol 20% (competitive substrate for alcohol dehydrogenase, bloc conversion to toxic metabolites)
• hemodialysis (remove EG and toxic metabolites)
• [note: decontamination NOT helpful]